van Loo Unit - Cellular and Molecular (Patho)physiology

Research Field: Study of in vivo mechanisms of inflammation-driven autoimmune pathology

Group leader: Prof. Dr. Geert van Loo

Tel: +32 9 33 13 761 - Fax: +32 9 221 76 73
Email: Geert.vanLoo.spam.detractor@irc.vib-UGentspam.corruptor.be

Research topic

Our research aims to understand the in vivo mechanisms by which inflammation drives (autoimmune) pathology. One major focus concerns the transcription factor NF-κB and the molecular mechanisms by which NF-κB controls inflammatory and apoptotic responses in vivo. Also ER stress and autophagy are being studied in this context, since more and more evidence indicates that also these pathways may be crucially involved in inflammatory reactions and the development of inflammatory pathology. For these studies we use transgenic mice as a model to study gene function in vivo, both through Cre/LoxP-mediated gene targeting allowing tissue-specific gene deletion, and through CRISP/Cas technology to introduce specific mutations in vivo. These mice are characterized in several mouse models of chronic inflammatory pathology, including models for inflammatory bowel disease, rheumatoid arthritis, diabetes, and multiple sclerosis.

Areas of expertise

  • ER stress and NF-κB signaling
  • In vivo mouse gene targeting and development of mouse models of inflammatory disease
  • Study of the molecular interplay between NF-κB, ER stress and autophagy in tissue homeostasis and inflammatory disease development

Technology transfer potential

  • Novel mouse models for inflammatory diseases
  • Therapeutic targets in inflammation and autoimmunity

Selected publications

  1. Vande Walle, et al. Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis.
    Nature. 512, 69-73, 2014.
  2. Vereecke, et al. A20 controls intestinal homeostasis through cell-specific activities.
    Nat Comm. 5, 5103, 2014.
  3. Slowicka, K., et al. Optineurin deficiency in mice is associated with increased sensitivity to Salmonella but does not affect proinflammatory NF-kB signaling.
    Eur. J. Immunol, 46, 971-980, 2016.
  4. Matmati M et al. A20 (TNFAIP3) deficiency in myeloid cells triggers erosive polyarthritis resembling rheumatoid arthritis. Nature Genetics, 43, 908-912, 2011.
  5. Vereecke L et al. Enterocyte specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis. Journal of Experimental Medicine, 207, 1513-1523, 2010.

Myelinated axons in brain corpus callosum


Mucus produced by intestinal goblet cells preventing bacterial adhesion in the colon

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